The chronic fatigue syndrome (CFS) has been recognized as an illness characterized by easy fatigability, prolonged lassitude and disturbances of sleep, sometimes but not always appearing to follow symptoms of an acute viral illness [Holmes et al, Ann Intern Med 108(3), 387-389 (1988) and Buchwald et al, JAMA 257(17), 2303-2307 (1987)]. Originally thought to be due to chronic Epstein Barr virus infection, this cause of CFS has been largely discredited [Koo, D., West J Med 150(50), 590-596 (1989)].
Recent observations indicate that one of the most prominent features of this syndrome is cognitive impairment. Although this impairment has been reported by patients and verified anecdotally by their physicians, it has not been quantified. No national survey of the frequency of the disease has been performed, but one report indicated the syndrome was common in general medicine practices [Buchwald et al, JAMA 257(17), 2303-2307 (1987)].
Peptide T has been shown to be associated with significant improvement in measurable cognitive function of persons with human immunodeficiency virus (HIV) [Bridge et al, Lancet II (8656), 226 (1989)].
In recent work, protein kinase A activity in humans has been shown to be increased by Peptide T. This enzyme system subserves the activity of the cyclic AMP system, the second order messenger system for a number of central nervous system functions including memory and circadian rhythmicity. Reductions in activity of this enzyme have been observed in chronic fatigue syndrome patients, and Peptide T increases pka activity in the same in vitro tests. These observations suggest that the effects of Peptide T seen in earlier HIV studies are related more generally to virally infected persons, and not restricted to HIV infections alone.